Borderline personality disorder (BPD)

1.1.1. Definition

Borderline personality disorder (BPD) is a complex and serious mental disorder, which is characterised by a marked impulsivity and a pervasive pattern of instability in interpersonal relationships, self-image and affects. It is associated with severe functional impairment, substantial treatment utilization, and a high mortality rate by suicide. Mortality rate in BPD patients is almost 10% to 50% times higher than the rate in the general population. The set of problems is manifested in a broad range of situations and life contexts and usually has its onset by late adolescence or early adulthood. In the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) (American Psychiatric Association, 2004), nine diagnostic criteria for BPD are listed (Table 1), out of which five have to be applied for a BPD diagnosis.

Diagnostic criteria for Borderline Personality Disorder

A pervasive pattern of instability of interpersonal relationships, self-image, and affects, and marked impulsivity beginning by early adulthood and present in a variety of contexts, as indicated by five (or more) of the following:

(1) frantic efforts to avoid real or imagined abandonment

(2) a pattern of unstable and intense interpersonal relationships characterized by alternating between extremes of idealization and devaluation

(3) identity disturbance: markedly and persistently unstable self-image or sense of self

(4) impulsivity in at least two areas that are potentially self-damaging (e.g., spending, sex, substance abuse, reckless driving, binge eating)

(5) recurrent suicidal behaviour, gestures, or threats, or self-mutilating behaviour

(6) affective instability due to a marked reactivity of mood (e.g. intense episodic dysphoria, irritability, or anxiety usually lasting a few hours and only rarely more than a few days)

(7) chronic feelings of emptiness

(8) inappropriate, intense anger or difficulty controlling anger (e.g., frequent displays of temper, constant anger, recurrent physical fights)

(9) transient, stress-related paranoid ideation or severe dissociative symptoms

Table 1: DSM-IV: Diagnostic criteria for Borderline Personality Disorder (American Psychiatric Association, 2004).

5 1.1.2. Epidemiology

Prevalence of BPD in the general population is greater than initially assumed. While Torgersen, Kringlen and Cramer (2001) estimated 1% to 2% of the general population to be affected, Grant et al.

(2008) estimated 5.9% to be affected. In most epidemiologic surveys prevalence of BPD does not differ by sex (Coid, Yang, Tyrer, Roberts, & Ullrich, 2006; Grant et al., 2008; Jackson & Burgess, 2000;

Lenzenweger, Lane, Loranger, & Kessler, 2007; Torgersen, Kringlen, & Cramer, 2001), but it often does in clinical studies (Widiger, 1998; Widiger & Weissman, 1991).

Clinical studies have shown BPD to be highly comorbid with other psychiatric disorders (Grant, et al., 2008; Oldham et al., 1995; Skodol et al., 1999; Zanarini et al., 1998a, 1998b; Zimmerman & Mattia, 1999). Looking for comorbidities in BPD patients Grant et al. (2008) found similar rates for lifetime and 12-month co-occurrence of other psychiatric disorders, respectively. Highest rates were found for panic disorder with agoraphobia, bipolar disorder I, and drug dependence. A little bit lower, but still high rates were found for mood disorders, anxiety, and substance use disorders (Table 2) (Grant, et al., 2008).

Lifetime co-occurrence 12-month co-occurrence

Panic disorder with

agoraphobia 36.0% 51.0%

Bipolar disorder I 35.9% 55.1%

Drug dependence 30.9% 45.8%

Mood disorders 17.2% 29.4%

Anxiety disorders 14.8% 21.5%

Substance use

disorder 9.5% 14.7%

Table 2: Lifetime and 12-month co-occurrence of other psychiatric disorders in BPD patients (Grant, et al., 2008)

Risk factors for BPD are believed to be both biological and environmental. While some scientists plead for genetic inheritance of neurobiological abnormalities, others focus on a history of adverse experience (Gunderson & Hoffman, 2005).

Lieb, Zanarini, Schmahl, Linehan and Bohus (2004) proposed a complex neurobehavioral model for the cause of BPD (Figure 1). This model involves several factors, which interact in various ways with each other. For example, genetic factors and adverse childhood experiences are considered to be causes for emotional dysregulation and impulsivity. Thus, they have an impact on dysfunctional behaviour, and psychosocial conflicts and deficits. These facts again may reinforce emotional dysregulation and impulsivity (Lieb, Zanarini, Schmahl, Linehan, & Bohus, 2004).

6

Figure 1: Neurobehavioral model for the cause or BPD (Lieb, et al., 2004).

Clinical studies suggest that environmental factors play an important role in the genesis of BPD. 71%

of BPD patients report the experience of severe childhood trauma (Lieb, et al., 2004). Various types of childhood adversity and traumatic life events are experienced by many patients. BDP patients showed a significantly higher rate of traumas, such as physical abuse (71%), sexual abuse (68%), and witnessing serious domestic violence (62%) than non-BPD patients (Herman, Perry, & Vanderkolk, 1989). Comparing BDP patients with depressive patients, the former reported a significant higher frequency of sexual abuse than the later (p=0.005) (Ogata et al., 1990). Compared to healthy control subjects, BPD patients experienced significantly more often early traumatic life events including sexual abuse, violence in the family, loss of mother, father or parents, childhood illness, etc.

(Bandelow et al., 2005).

Genetic studies, which provide evidence for genetic factors as a cause for BPD, are rare.

Notwithstanding, conducting a twin study, Torgersen et al. (2000) found concordance for definite BPD of 35% in monozygotic twin pairs and only 7% in dizygotic pairs. This obviously implies a genetic component in BDP (Torgersen et al., 2000).

1.1.3. Therapy

There are several psychotherapeutic approaches to treat BPD. However, one of the most studied and most efficient cognitive behavioural psychotherapies is the so called dialectic behaviour therapy (DBT) (M. Linehan, 1993a, 1993b). Many authors showed that compared with treatment-as-usual, DBT reduces effectively core symptoms of BDP (Bohus et al., 2004; Bohus et al., 2000; M. M. Linehan, Armstrong, Suarez, Allmon, & Heard, 1991; M. M. Linehan et al., 2006). The standard DBT program was originally developed for outpatients, chronically parasuicidal and meeting criteria for BPD. The hierarchically arranged goals of the DBT are far-reaching. They include (1) the reduction of suicidal behaviour, (2) of behaviours that interfere with treatment delivery and (3) of other dangerous, severe, or destabilizing behaviours. Furthermore, they comprise of (4) acquiring behavioural skills, (5) decreasing posttraumatic stress responses related to previous traumatic events, (6) increasing self-respect and lastly (7) meeting other goals of the patient is comprised. To best reach these goals the following four service modes are provided: (1) weekly individual psychotherapy for 1 hour per week, (2) 2½ hours group skills training per week, (3) telephone consultation (as needed within the therapist’s limits to ensure generalization), and (4) weekly therapist consultation team meetings to enhance therapist motivation and skills (M. Linehan, 1993a, 1993b; M. M. Linehan, et al., 2006).

7 McQuillan et al. (2005) have developed a shortened intensive version of the standard DBT. The intensive dialectical behaviour therapy (I-DBT) was found to be an effective treatment, which offers the essential components of the standard DBT within 3 weeks: individual and group therapy and limited phone call availability of the therapists between 8:30 a.m. and 6:00 p.m. (McQuillan et al., 2005).